Name: Acetylsalicylic Acid/Aspirin
Class: Salicylate
Mech.: Irrevers. acetylation of cyclooxygenase → inhib. of prostaglandin synth.
→ ↓ prostaglandins, thromboxanes, & prostacyclins → analgesia, inhib. of
platelet aggregation, anti-inflammatory effects, anti-pyresis, stim. of central
resp. center.
Absorption: Rapidly absorbed in stomach and upper intestine. Also absorbed
through skin. pKa = 3.5, so gastric acid → ↑ absorption. Enteric coating
may delay absorption.
Dist.: pH-dependent passive (non-ionic) diffusion. Active transport in renal
tubules. 90% bound to albumin.
Metab.: Hydrolyzed by tissue/blood esterases. Conjugated in liver.
Excretion, t_: Salicylate & metabolites excreted in urine. pH-dependent—30%
excretion in alkaline urine, 2% in acidic urine. Low doses (600 mg) = 1st order;
t_ = 3-5 hr. High doses (4 g/d) = 0 order, t_ = 15 hr.
Utility: Analgesia—mild-mod. pain, somatic pain. No dependence or tolerance.
Low efficacy for visceral pain. Anti-inflammatory—also a mech. of analgesia.
Anti-pyresis—inhib. bacterial pyrogens in CNS; blocks hypothalamic response
to IL-1. ↓ Platelet aggregation—2° to inhib. of thromboxane synth.
Name: Methylsalicylate (Oil of Wintergreen)
Class: Salicylate
Mech.:
Absorption: Absorbed transdermally.
Dist.:
Metab.:
Excretion, t_:
Toxicity/S.E.s: Used in foods…may be toxic.
Utility: Used in liniments for cutaneous counterirritation.
Special Features:
1 www.brain101.info
Aspirin cont.
Toxicity/S.E.s: GI bleeding and ulceration—usu. due to high doses, but may
occur w/lower doses. Painless bleeding may cause iron-deficiency anemia.
Hypersensitivity—usu. in patients w/nasal polyps, asthma, or chronic urticaria
→ urticaria, angioedema, hypotension. Bleeding—C/i w/severe hepatic damage,
vit. K deficiency, hemophilia. Hepatotoxicity w/CT disorders. May be involved
in Reye’s Synd.; not recommended for kids w/chicken pox or influenza.
Pregnancy—reduced birth weight, ↑ perinatal mortality, ante/post-partum
hemorrhage, prolonged gestation. Renal effects—low doses → ↓ uric acid
excretion; high doses → ↑ uric acid excretion. Poisoning—acute → resp.
alkalosis (hyperventilation), metabolic acidosis (fixed anion). Correlates
w/plasma conc. Chronic → higher brain conc. than in acute poisoning; greater
toxicity than plasma conc. would suggest. More resistant to treatment than
acute poisoning.
Drug Interactions: Alcohol → ↑ gastric bleeding. Displacement of oral
hypoglycemia drugs, NSAIDS, methotrexate, phenytoin, oral anti-coagulants, &
sulfonamides from protein binding sites.
Special Features: May exacerbate acute gout attacks.
Name: Salicylamide
Class: Salicylate
Mech.:
Absorption:
Dist.:
Metab.:
Excretion, t_:
Toxicity/S.E.s:
Utility:
Special Features: May exacerbate acute gout attacks.
???
Name: Ibuprofen (Advil, Motrin, Nuprin) (OTC)
Class: NSAID
Mech.: Inhibition of cyclooxygenase → inhibition of prostaglandin synthesis. Also inhib. of PMN
adhesion, aggregation, & activation (ramifications uncertain).
Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 1-2 hr.
Dist.: Weak acid (pKa <5). ~90% protein binding. Vd ≅ albumin Vd.
Metab.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).
Excretion, t_: Metabolites in urine. Renal failure → retention of glucuronide metabolites → potential
for toxic accumulation of orig. compound. t_ = 2-3 hr.
Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration,
hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon
hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible
cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic
renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis.
Overdose—Acute is less serious than w/aspirin, but may cause metabolic acidosis & seizures.
Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.
Name: Sulindac (Clinoril)
Class: NSAID
Mech.: Inhibition of cyclooxygenase → inhibition of prostaglandin synthesis. Also inhib. of PMN
adhesion, aggregation, & activation (ramifications uncertain).
Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 1-2 hr.
Dist.: Weak acid (pKa <5). ~90% protein binding. Vd ≅ albumin Vd.
Metab.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).
Excretion, t_: Metabolites in urine, bile, feces. Renal failure → retention of glucuronide metabolites
→ potential for toxic accumulation of orig. compound. t_ = 8-16 hr. Decreased clearance
w/hepatic impairment and in the elderly.
Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration,
hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon
hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible
cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic
renal failure, interstitial nephritis, but less likely to cause kidney effects than other NSAIDs.
CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than
w/aspirin, but may cause metabolic acidosis & seizures.
Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.
Special Features: Pro drug (converted to an active metabolite).
2 www.brain101.info
Name: Indomethacin (Indocin)
Class: NSAID
Mech.: Inhibition of cyclooxygenase → inhibition of prostaglandin synthesis. Also inhib. of PMN
adhesion, aggregation, & activation (ramifications uncertain).
Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 1-2 hr.
Dist.: Weak acid (pKa <5). ~90% protein binding. Vd ≅ albumin Vd.
Metab.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).
Excretion, t_: Metabolites in urine, bile, & feces. Renal failure → retention of glucuronide
metabolites→potential for toxic accum. of orig. compound. t_=4-5 hr. Decreased clearance
w/hepatic/renal impairment & in the elderly.
Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration,
hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon
hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-
reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic renal
failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis.
Overdose—Acute is less serious than w/aspirin, but may cause metabolic acidosis & seizures.
Use limited by toxicity. 100% cross-reactivity with aspirin.
Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.
Special Features: Most commonly used NSAID for acute gout attack due to short peak time & rapid
clearance.
Name: Flurbiprofen (Ansaid)
Class: NSAID
Mech.: Inhibition of cyclooxygenase → inhibition of prostaglandin synthesis. Also inhib. of PMN
adhesion, aggregation, & activation (ramifications uncertain).
Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 1-5 hr.
Dist.: Weak acid (pKa <5). ~90% protein binding. Vd ≅ albumin Vd.
Metab.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).
Excretion, t_: Metabolites in urine. Renal failure → retention of glucuronide metabolites → potential
for toxic accumulation of orig. compound. t_ = 5 hr.
Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration,
hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon
hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible
cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic
renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis.
Overdose—Acute is less serious than w/aspirin, but may cause metabolic acidosis & seizures.
Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.
Name: Naproxen (Naprosyn)
Class: NSAID
Mech.: Inhibition of cyclooxygenase → inhibition of prostaglandin synthesis. Also inhib. of PMN
adhesion, aggregation, & activation (ramifications uncertain).
Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 2-4 hr.
Dist.: Weak acid (pKa <5). ~90% protein binding. Vd ≅ albumin Vd.
Metab.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).
Excretion, t_: Metabolites in urine. Renal failure → retention of glucuronide metabolites→potential
for toxic accumulation of orig. compound. t_ = 12-15 hr. Clearance decreased w/renal/hepatic
impairment & in the elderly.
Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration,
hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon
hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible
cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic
renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis.
Overdose—Acute is less serious than w/aspirin, but may cause metabolic acidosis & seizures.
Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.
Name: Diflunisal (Dolobid)
Class: Salicylate.
Mech.: Inhibition of cyclooxygenase → inhibition of prostaglandin synthesis. Also inhib. of PMN
adhesion, aggregation, & activation (ramifications uncertain).
Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 2-3 hr.
Dist.: Weak acid (pKa <5). ~90% protein binding. Vd ≅ albumin Vd. No CNS.
Metab.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).
Excretion, t_: Metabolites in urine. Renal failure → retention of glucuronide metabolites→potential
for toxic accumulation of orig. compound. t_ = 11-15 hr. Clearance decreased w/renal
impairment & in the elderly.
Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration,
hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon
hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible
cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic
renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis.
Overdose—Acute is less serious than w/aspirin, but may cause metabolic acidosis & seizures.
Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.
Special Features: Not metab. to salicylate, ∴ no salicylate intoxication. No CNS → no antipyretic
properties. 3-4x more potent than aspirin.
3 www.brain101.info
Name: Piroxicam (Feldene)
Class: NSAID
Mech.: Inhibition of cyclooxygenase → inhibition of prostaglandin synthesis. Also inhib. of PMN
adhesion, aggregation, & activation (ramifications uncertain).
Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 3-5 hr.
Dist.: Weak acid (pKa <5). ~90% protein binding. Vd ≅ albumin Vd.
Metab.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).
Excretion, t_: Metabolites in urine. Renal failure → retention of glucuronide metabolites→potential
for toxic accumulation of orig. compound. t_ = 30-86 hr.
Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration,
hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon
hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible
cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic
renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis.
Overdose—Acute is less serious than w/aspirin, but may cause metabolic acidosis & seizures.
Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.
Name: Ketorolac (Toradol)
Class: NSAID
Mech.: Inhibition of cyclooxygenase → inhibition of prostaglandin synthesis. Also inhib. of PMN
adhesion, aggregation, & activation (ramifications uncertain).
Absorption: Parenteral only.
Dist.: Weak acid (pKa <5). ~90% protein binding. Vd ≅ albumin Vd.
Metab.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).
Excretion, t_: Metabolites in urine. Renal failure → retention of glucuronide metabolites → potential
for toxic accumulation of orig. compound.
Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration,
hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon
hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible
cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na+ retention, hemodynamic
renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis.
Overdose—Acute is less serious than w/aspirin, but may cause metabolic acidosis & seizures.
Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout. May be as
effective as morphine or meperidine for short-term relief of mod.-severe pain.
Name: Gold (Auranofin, Aurothioglucose) Name: D-penicillamine (Cuprimine)
Class: Slow-Acting Antirheumatic Agent Class: Slow-Acting Antirheumatic Agent
Mech.: Unknown. May involve alteration of macrophage fxn. Mech.: Unknown. Suppresses/modifies immune system & interacts w/leukocyte
Absorption: Auranofin—oral. Aurathioglucose—IM. membrane receptors. Also chelates heavy metals (e.g., Pb, Hg, As, Cu).
Dist.: 95% protein bound. Absorption: Oral.
Metab.: Dist.: 80% protein bound.
Excretion, t_: 65% in urine, 35% feces. 5-6 days. Metab.:
Toxicity/S.E.s: Affects about 1/3 of patients. Mucocutaneous—pruritis & Excretion, t_: Urine.
dermatitis. Renal—proteinuria, nephrotic synd., hematuria. Toxicity/S.E.s: Mucocutaneous—pruritis, dermatitis. Renal—proteinuria,
Hematologic—eosinophilia, thrombocytopenia, aplastic anemia. nephrotic synd. Hematologic—thrombocytopenia, aplastic anemia.
Utility: Treatment of patients w/rheumatoid arthritis who are unresponsive to Pulmonary—hemorrhagic pneumonitis.
NSAIDs or whose symptoms persist despite maximal tolerated doses of Utility: Treatment of patients w/rheumatoid arthritis who are unresponsive to
NSAIDs. NSAIDs or whose symptoms persist despite maximal tolerated doses of
Special Features: NSAIDs.
Special Features:

Name: Methotrexate (Rheumatrex) Name: Hydroxychloroquine (Plaquenil)

Class: Slow-Acting Antirheumatic Agent (Antimetabolite)
Class: Slow-Acting Antirheumatic Agent (Anti-Malarial Agent)
Mech.: Inhib. dihydrofolate reductase → inhib. of formation of tetrahydrofolic acid
Mech.: Unknown. Inhib. nucleic acid synth, stabilizes lysosomal membranes,
→ ↓ synth of purines, thymidylic acid, methionine, and serine → traps free radicals.
↓ DNA/RNA/protein synth. → eventual cell death. Absorption:
Absorption: Oral, IV, IM, IT.
Dist.: No CNS unless administered IT. Dist.:
Metab.: Excretion, t_: Metab.:
Toxicity/S.E.s: Stomatitis, myelosuppression, erythema, rash, urticaria, alopecia, Excretion, t_:
n/v/d. Long term use may → hepatic fibrosis. High doses may → Toxicity/S.E.s: GI upset, pruritis, headaches, visual disturbances, discoloration
crystalluria. Patient must be well hydrated and have alkaline urine to avoid of nail beds and mucous membranes.
renal toxicity. Also pulmonary toxicity in children. IT admin. → subacute Utility: Treat rheumatoid arthritis that has been unresponsive to NSAIDs. Also
meningeal irritation, stiff neck, headache, fever; rarely seizures, used to treat rheumatoid arthritis in conjunction w/an NSAID (allows use of
encephalopathy, paraplegia. C/i w/pregnancy (teratogenic). lower dose of hydroxychloroquine).
Utility: Low doses useful in treating rheumatoid arthritis and severe psoriasis.
Special Features:
Effective against acute lymphocytic leukemia, choriocarcinoma, Burkitt’s
lymphoma, breast cancer, head/neck carcinomas. High doses are
curative for osteogenic sarcoma and choriocarcinoma.

4 www.brain101.info
Name: Sulfasalazine (Azulfidine) Name: Levamisole (Ergamisol)
Class: Sulfonamide (Slow-Acting Antirheumatic Agent) Class: Slow-Acting Antirheumatic Agent (Veterinary Anti-Helminthic Agent)
Mech.: Comp. inhib. of PABA incorp. into dihydropteric acid → inhib. of folic acid. Mech.: Enhances cell-mediated immune responses (↑ chemotaxis &
Absorption: Poorly absorbed in GI tract. phagocytosis of PMNs and Mφs, ↑ T cell fxn). How these effects
Distribution: GI tract ameliorate RA is unknown.
Metab.: Hydrolyzed to active form by intest. bacteria. Absorption:
Excretion, t_: feces Dist.:
Metab.:
Toxicity/S.E.s: Interferes w/normal flora → ↓ vit. K synth.
Excretion, t_:
Utility: Active in bowel lumen. Used prior to surgery to reduce microbe
population. Treat inflammatory bowel disease, rheumatoid arthritis. Toxicity/S.E.s: Rash (most common), leukopenia, agranulocytosis,
thrombocytopenia, influenza-like illnesses, mouth ulcers, n/v.
Special Features: Broken down in intestines to liberate 5-aminosalicylate (anti-
inflammatory). Utility: Treat rheumatoid arthritis (off-label use).
Special Features:

Name: Probenecid (Benemid) Name: Sulfinpyrazone (Anturane)

Class: Anti-Gout Agent (Uricosuric Agent)
Mech.: Blocks proximal tubular reabsorption of uric acid.
Absorption:
Dist.:
Metab.:
Excretion, t_: Reabsorbed by renal tubules & metabolized slowly.
Toxicity/S.E.s: GI irritation (not severe). Skin rash. Rare aplastic anemia.
Utility: Treat gout via increased urinary excretion of uric acid. Blocks tubular
secretion of penicillin; may be used to increase penicillin levels.
Special Features: At low doses, probenecid blocks proximal tubule secretion of
uric acid.
Class: Anti-Gout Agent (Uricosuric Agent)
Mech.: Blocks proximal tubular reabsorption of uric acid.
Absorption:
Dist.:
Metab.:
Excretion, t_: Rapidly excreted by the kidneys.
Toxicity/S.E.s: GI irritation (not severe). Skin rash. Rare aplastic anemia.
Utility: Treat gout via increased urinary excretion of uric acid.
Special Features: At low doses, sulfinpyrazone blocks proximal tubule secretion
of uric acid.

5 www.brain101.info
Name: Allopurinol (Zyloprim)
Class: Anti-Gout Agent
Mech.: Inhibits xanthine oxidase → ↓ production of uric acid.
Absorption: Well absorbed orally.
Dist.:
Metab.: Metab. by xanthine oxidase to a longer acting active metabolite.
Excretion, t_:
Toxicity/S.E.s: GI intolerance, skin rash.
Drug Interactions: Inhib. metab. of oral anticoagulants. Xanthine oxidase
inactivates 6-mercaptopurine & azathioprine (cancer chemotherapeutic
drugs). ∴ doses must be lowered when patient takes allopurinol.
Utility: Treat chronic tophaceous gout, gout patients w/high excretion of uric
acid, patients who cannot use probenecid or sulfinpyrazone, recurrent
renal uric acid stones, renal impairment, grossly elevated serum acid
concentrations (>13 mg/dL). Use also w/cancer chemotherapy to prevent
urate nephropathy.
Special Features:
Name: Acetaminophen (Tylenol)
Class: Para-aminophenol (OTC)
Mech.: Weak inhib. of peripheral prostaglandin synth. More effective CNS
cyclooxygenase inhib. → antipyretic and analgesic properties.
Absorption: Oral → rapid & complete w/peak in 30-60 min. Not a weak acid.
Dist.: Dist. throughout body fluids. Protein binding (20-50%) not significant.
Metab.: No zero-order kinetics. Phase II conjug. w/glucuronic acid & sulfate.
Phase I oxid. → N-acetyl-benzoquinoneimine. Reacts w/sulfhydryl
groups, but normally inactivated by glutathione (except in overdose).
Excretion, t_: Majority excreted as conjug. metabolites in urine. Not related to
urine pH. 2 hr.
Toxicity/S.E.s: Overdose → depletion of hepatic glutathione → rxn. w/sulfhydryl
groups of hepatic proteins → hepatic necrosis. Also renal tubular
necrosis. Treatment w/N-acetylcysteine w/in 10 hr. of overdose can be
life-saving.
Utility: Analgesic and antipyretic efficacies comparable to aspirin.
Special Features: Para-aminophenol prototype. Often used w/other analgesics
(e.g., Tylenol + Codeine). Weak peripheral inhib. → weak anti-
inflammatory activity. No urocosuric or anti-platelet effects.
6 www.brain101.info
Name: Colchicine
Class: Anti-Gout Agent
Mech.: Binds to tubulin → inhib. of leukocyte migration & phagocytosis →
↓ inflamm. response.
Absorption: Rapidly absorbed orally.
Dist.:
Metab.:
Excretion, t_: Urine & feces.
Toxicity/S.E.s: GI intolerance (n/v/d).
Utility: Treat acute gout attacks. Use to prevent acute attacks while initiating
allopurinol or probenecid therapy.
Special Features: Not analgesic. No effect on uric acid production or excretion.
Name: Phenacetin
Class: Para-aminophenol
Mech.: Converted to acetaminophen. Weak inhib. of peripheral prostaglandin synth. More effective
CNS cyclooxygenase inhib. → antipyretic and analgesic properties.
Absorption: Oral → rapid & complete. Not a weak acid.
Dist.: Dist. throughout body fluids. Protein binding (20-50%) not significant.
Metab.: No zero-order kinetics. Phase II conjug. w/glucuronic acid & sulfate. Phase I oxid. → N-
acetyl-benzoquinoneimine. Reacts w/sulfhydryl groups, but normally inactivated by
glutathione (except in overdose).
Excretion, t_: Majority excreted as conjug. metabolites in urine. Not related to urine pH.
Toxicity/S.E.s: Nephropathy assoc. w/chronic use. Overdose → depletion of hepatic glutathione →
rxn. w/sulfhydryl groups of hepatic proteins → hepatic necrosis. Also renal tubular
necrosis. Treatment w/N-acetylcysteine w/in 10 hr. of overdose can be life-saving.
Utility: Analgesic and antipyretic efficacies comparable to aspirin.
Special Features: No longer prescribable in US due to renal toxicity. Weak peripheral inhib. →
weak anti-inflammatory activity. No urocosuric or anti-platelet effects.
Name: Cyclosporine (Sandimmune) Name: OKT3 (Muromonab-CD3)
Class: Immunosuppressant
Class: Immunosuppressant
Mech.: Binds to calmodulin and a cytoplasmic cytophilin → selective inhib. of
Mech.: Opsonizes T cells, modulates CD3 antigen recognition complex on T cells,
transcription of IL-2 gene → inhib. of IL-2 prod. & release from T4 cells, blocks CTL killer function.
inhib. of proliferation of T8 cells, block of T4 activation of B cells.
Absorption: IV
Absorption: Oral → highly variable and incomplete absorption.
Dist.: Large Vd. Binds in tissues. 60-70% contained in RBCs. Dist.:
Metab.: Extensive hepatic metab involving cyt. P450 enzymes. 17 metabolites Metab.:
known. Drug levels monitored by RIA or HPLC. Excretion, t_:
Excretion, t_: Biliary excretion, minor renal excretion.
Toxicity/S.E.s: Chills, fever, thrombocytopenia, erythema, pruritis,
Toxicity/S.E.s: Nephrotoxicity (main toxicity), hepatotoxicity, hirsutism, gingival
hyperplasia, neurotoxicity, altered coagulability. But little (if any) hypersensitivity rxns, anti-OKT3 antibody production (∴ only given
bone marrow suppression. Drug interactions—rifampin & for 1-2 weeks).
phenobarbital → induction of hepatic metab. Erythromycin → Utility: Prevent or reverse acute allograft rejection.
inhib. of hepatic metab. Ketoconazole & amphotericin → ↓ Special Features: Murine monoclonal antibody against CD3 on T cells.
clearance.
Utility: Prolong organ transplants (1° use). Suppress cell-med. diseases.
Possible benefit w/early treatment of IDDM.
Special Features:

Name: Prednisone Name: Methylprednisone

Class: Corticosteroid (Immunosuppressant) Class: Corticosteroid (Immunosuppressant)
Mech.: Inhib. of IL-1 & TNF synth/release from Mφs → ↓ activation of T cells and Mech.: Inhib. of IL-1 & TNF synth/release from Mφs → ↓ activation of T cells and
Mφs, ↓ PMN fxn, ↓ T cell-dependent Ab production, ↓ complement Mφs, ↓ PMN fxn, ↓ T cell-dependent Ab production, ↓ complement
activity, ↓ activity & release of kinins. activity, ↓ activity & release of kinins.
Absorption: Oral Absorption: Parenteral
Dist.:
Dist.:
Metab.:
Metab.:
Excretion, t_:
Excretion, t_:
Toxicity/S.E.s: Suppressed pituitary adrenal fxn, hypertension, weight gain,
peptic ulcer, GI bleeding, euphoric personality changes, cataracts, Toxicity/S.E.s: Suppressed pituitary adrenal fxn, hypertension, weight gain,
hyperglycemia. peptic ulcer, GI bleeding, euphoric personality changes, cataracts,
Utility: Immunosuppression. Primarily employed to induce remission in patients hyperglycemia.
w/acute lymphocytic leukemia, and for treatment of lymphomas. Treat Utility: Immunosuppression. Primarily employed to induce remission in patients
hypercalcemia due to vit. D intox., sarcoidosis, or specific cancers (e.g., w/acute lymphocytic leukemia, and in treatment of lymphomas.
lymphoproliferative) (30-60 mg/d). Special Features:
Special Features:

7 www.brain101.info
Name: Azathioprine (Imuran) Name: Cyclophosphamide (Cytoxan)
Class: Immunosuppressant (Antimetabolite) Class: Immunosuppressant (Alkylating Agent) (Cancer Chemotherapeutic Agent)
Mech.: Converted to 6-mercaptopurine (thiol analog of hypoxanthine) → inhib. of Mech.: Activated via hepatic P450 metabolism → phosphoramide mustard.
purine synth. → cytotoxicity to dividing cells → ↓ lymphocyte proliferation Phosphoramide mustard alkylates DNA → cytotoxicity to dividing cells.
→ inhib. of cellular and humoral immunity. Absorption: Oral
Absorption: Dist.:
Dist.: Metab.:
Metab.: Excretion, t_:
Excretion, t_: Toxicity/S.E.s: Bone marrow depression (esp. leukocytosis), hemorrhagic
Toxicity/S.E.s: Bone marrow depression (main toxicity), n/v/d, hepatotoxicity. cystitis (may → bladder fibrosis), n/v/d, alopecia, amenorrhea,
Utility: Primarily used in maintenance of remission in acute lymphoblastic testicular atrophy, sterility. Possible secondary malignancies
leukemia. years later.
Special Features: Utility: Cancer chemotherapy, nephrotic syndrome, intractable rheumatoid
arthritis.
Special Features: Therapeutic effect independent of level of P450 activity.

Name: Antilymphocyte Globulin (ALG) Name: G-CSF (Filgrastim)

Class: Immunosuppressant Class: Immunostimulant
Mech.: Polyclonal antibody to human lymphocytes (not selective to CD3) → Mech.: Promotes growth & differentiation of granulocyte precursors.
destruction and inactivation of lymphocytes. Absorption:
Absorption: Dist.:
Dist.: Metab.:
Metab.: Excretion, t_:
Excretion, t_: Toxicity/S.E.s: Bone pain, fever, anti-CSF antibodies.
Toxicity/S.E.s: Chills, fever, thrombocytopenia, erythema, pruritis, Utility: Restore hematopoiesis (FDA-approved to treat neutropenia), augment
hypersensitivity rxns, anti-ALG antibody production (∴ only given host defenses, esp. after cancer therapy.
for 1-2 weeks). Special Features:
Utility: Prevent or reverse acute allograft rejection.
Special Features:

8 www.brain101.info
Name: GM-CSF (Sargramostim) Name: Erythropoietin (Epoetin Alfa, Epogen)
Class: Immunostimulant Class: Immunostimulant
Mech.: Stim. bone marrow production of precursors to PMNs, monocytes, Mech.: Stim. division/differentiation of erythroid progenitors in bone marrow.
platelets. Also activates PMNs, eosinophils, and monocytes. Absorption:
Absorption: Dist.:
Dist.: Metab.:
Metab.: Excretion, t_:
Excretion, t_: Toxicity/S.E.s: Usu. well-tolerated. Low incidence of hypertension, headache,
Toxicity/S.E.s: Fever, dermatologic rxns, splenomegaly. seizures. Rare hypersensitivity rxns.
Utility: FDA-approved to increase myeloid recovery rate after bone marrow Utility: Treat anemia assoc. w/chronic renal failure, AZT therapy, cancer and
transplantation. Also used for hematological reconstitution after chemotherapy. Supplemental iron eventually required in therapy.
autologous bone marrow transplants and treatments w/bone marrow Special Features: Manufactured by recombinant DNA technology. Identical to
cytotoxic drugs. human erythropoietin.
Special Features: Greater severity of immunologic S.E.s than w/G-CSF.

Name: Interferon α Name: Interferon β

Class: Immunostimulant Class: Immunostimulant
Mech.: Binds to cell-surface receptors → inhib. of viral replication, inhib. of cell Mech.: Binds to cell-surface receptors → inhib. of viral replication, inhib. of cell
proliferation. proliferation.
Absorption: Absorption:
Dist.: Dist.:
Metab.: Metab.:
Excretion, t_: Excretion, t_:
Toxicity/S.E.s: Fever w/chills; dose-related leukopenia, thrombocytopenia; Toxicity/S.E.s: Fever w/chills; dose-related leukopenia, thrombocytopenia;
fatigue, malaise, anorexia, weight loss, alopecia, transient fatigue, malaise, anorexia, weight loss, alopecia, transient
elevation of liver enzymes. High doses may → transient & elevation of liver enzymes. High doses may → transient &
reversible nephrotoxicity. reversible nephrotoxicity.
Utility: IFN α2A is approved for mgt. of hairy cell leukemia. Also useful for Utility: Used to treat for chronic hepatitis B, virally induced tumors, recurrent
chronic hepatitis B, virally induced tumors, recurrent varicella zoster, HSV varicella zoster, HSV keratitis, Kaposi’s sarcoma, hairy cell leukemia,
keratitis, Kaposi’s sarcoma, cutaneous T cell lymphoma. cutaneous T cell lymphoma.
Special Features: Produced by mononuclear leukocytes. Interferon production Special Features: Produced by fibroblasts. Interferon production is induced by
is induced by dsRNA (poly I:C), ampligen (mismatched dsRNA (poly I:C), ampligen (mismatched nucleotides), LPS.
nucleotides), LPS.

9 www.brain101.info
Name: Interferon γ Name: Bacillus Calumet-Guerin (BCG)
Class: Immunostimulant Class: Immunostimulant
Mech.: Binds to cell-surface receptors → activation of NK cells and Mφs, Mech.: Viable strain of Mycobaterium bovis. Enhances Mφ activity, promotes Mφ
promotion of conversion to TH1 cells. tumoricidal activity.
Absorption: Absorption:
Dist.: Dist.:
Metab.: Metab.:
Excretion, t_: Excretion, t_:
Toxicity/S.E.s: Fever w/chills; dose-related leukopenia, thrombocytopenia;
Toxicity/S.E.s:
fatigue, malaise, anorexia, weight loss, alopecia, transient
elevation of liver enzymes. High doses may → transient & Utility: Treat bladder carcinoma and melanomas.
reversible nephrotoxicity. Special Features:
Utility: Used to treat for chronic hepatitis B, virally induced tumors, recurrent
varicella zoster, HSV keratitis, Kaposi’s sarcoma, hairy cell leukemia,
cutaneous T cell lymphoma.
Special Features: Produced by memory TH1 cells and NK cells. Interferon
production is induced by dsRNA (poly I:C), ampligen
(mismatched nucleotides), LPS.

Name: Misoprostol (Cytotec) How, if some day or night a demon were to sneak after you into your loneliest
Class: Gastric Protectant (Prostaglandin) loneliness and say to you, “This life as you now live it and have lived it, you
Mech.: Analog of prostaglandin E1. Inhib. secretion of HCl. Stimulates secretion will have to live once more and innumerable times more; and there will be
of mucus & HCO3 (cytoprotective). nothing new in it, but every pain and every joy and every thought and sigh and
Absorption: everything immeasurably small or great in your life must return to you - all in
Dist.: the same succession and sequence - even this spider and this moonlight between
the trees, and even this moment and I myself. The eternal hourglass of existence
Metab.:
is turned over and over, and you with it, a dust grain of dust.” Would you not
Excretion, t_: throw yourself down and gnash your teeth and curse the demon who spoke thus?
Toxicity/S.E.s: Diarrhea, nausea. Produces uterine contractions. ∴ c/i during Or did you once experience a tremendous moment when you would have
pregnancy. answered him, “You are a god, and never have I heard anything more godly.” If
Utility: Only agent approved for prevention of gastric ulcers induced by NSAIDs. this thought were to gain possession of you, it would change you, as you are, or
Less effective than H2 antagonists for acute treatment of peptic ulcers. perhaps crush you. The question in each and every thing, “Do you want this
Special Features: once more and innumerable times more?” would weigh upon your actions as the
greatest stress. Or how well disposed would you have to become to yourself and
to life to crave nothing more fervently than this ultimate eternal confirmation and
seal?
- Nietzsche

10 www.brain101.info